Dissecting the molecular mechanisms of DNA double-strand break repair

Dheva Setiaputra, PhD
Postdoctoral fellow
Lunenfeld-Tanenbaum Research Institute
Mount Sinai Hospital in Toronto

Special Conference: This speaker is a candidate for the Research Unit Director position available at the IRCM.

In person: 
IRCM Auditorium
110, avenue des Pins O, H2W 1R7 Montreal
Wearing a mask is mandatory at all times

Online:
Zoom Link : https://zoom.us/j/94078486709
ID : 940 7848 6709
Code : 785826

This conference is set to occur under a hybrid format. However, please note that last-minute changes to online-only lecture may occur due to unforeseen circumstances. We invite you to visit this webpage again a few days before attending.

About the conference:
DNA double-strand breaks (DSBs) are highly deleterious lesions that threaten genome stability. Homologous recombination and nonhomologous end-joining are two prominent mammalian DSB repair pathways that mutually antagonize to ensure faithful repair. The prototypical factors representing this antagonism are the end-joining factor 53BP1 and the homologous recombination factor BRCA1. Loss of 53BP1 was known to reverse many phenotypes of BRCA1 deficiency such as embryonic lethality and drug sensitivity. The mechanistic basis of 53BP1 suppression of homologous recombination was unknown. We used CRISPR screens to identify the shieldin complex that act downstream of 53BP1. Through a combination of biochemistry, cell biology, and computational approaches, I defined the mechanisms regulating their recruitment to and biochemical action at DSBs. These findings represent a key milestone in the quest to understand the nature of 53BP1-BRCA1 antagonism. I also embarked upon the preliminary steps in the biochemical dissection of a homologous recombination helicase that participates in DNA interstrand crosslink repair and meiotic DSBs.

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